Disparity in the Natural Cycles of <i>Borrelia burgdorferi</i> and the Agent of Human Granulocytic Ehrlichiosis

Levin, Michael; Vignes, Franka des; Fish, Durland

doi:10.3201/eid0502.990203

Cited by 45 publications

(51 citation statements)

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“…The agent of HGE is a newly described obligate intracellular pathogen with a tropism for the neutrophil (7). Coinfection with B. burgdorferi and the HGE agent has been documented in humans (1,7,48,71), ticks (20,59,70), and mice (49). However, the frequency of dual infection and its effect on the course of disease is not known.…”

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Coinfection withBorrelia burgdorferiand the Agent of Human Granulocytic Ehrlichiosis Alters Murine Immune Responses, Pathogen Burden, and Severity of Lyme Arthritis

et al. 2001

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Lyme disease and human granulocytic ehrlichiosis (HGE) are tick-borne illnesses caused by Borrelia burgdorferi and the agent of HGE, respectively. We investigated the influence of dual infection with B. burgdorferi and the HGE agent on the course of murine Lyme arthritis and granulocytic ehrlichiosis. Coinfection resulted in increased levels of both pathogens and more severe Lyme arthritis compared with those in mice infected with B. burgdorferi alone. The increase in bacterial burden during dual infection was associated with enhanced acquisition of both organisms by larval ticks that were allowed to engorge upon infected mice. Coinfection also resulted in diminished interleukin-12 (IL-12), gamma interferon (IFN-␥), and tumor necrosis factor alpha levels and elevated IL-6 levels in murine sera. During dual infection, IFN-␥ receptor expression on macrophages was also reduced, implying a decrease in phagocyte activation. These results suggest that coinfection of mice with B. burgdorferi and the HGE agent modulates host immune responses, resulting in increased bacterial burden, Lyme arthritis, and pathogen transmission to the vector.

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“…Dual infection involving B. burgdorferi and the HGE agent has been documented in humans and mice (7,49,52,56). In addition, ticks may be colonized by both pathogens (49,59).…”

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confidence: 99%

Coinfection withBorrelia burgdorferiand the Agent of Human Granulocytic Ehrlichiosis Alters Murine Immune Responses, Pathogen Burden, and Severity of Lyme Arthritis

et al. 2001

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“…Coinfection with both pathogens has been reported in humans (Ahkee & Ramirez, 1996;Bakken et al, 1996;Lebech et al, 1998), Ixodes ticks (Daniels et al, 1997;Pancholi et al, 1995;Telford et al, 1996) and wild rodents (Levin et al, 1999). In experimentally infected mice, the coinfection of A. phagocytophilum and B. burgdorferi sensu stricto resulted in increased levels of both pathogens and more severe Lyme arthritis compared with those in mice experimentally infected with B. burgdorferi sensu stricto alone (Thomas et al, 2001;Grab et al, 2007).…”

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confidence: 95%

Prevalence of Anaplasma phagocytophilum and its coinfection with Borrelia afzelii in Ixodes ricinus and Ixodes persulcatus ticks inhabiting Tver Province (Russia) – a sympatric region for both tick species

Masuzawa

Kharitonenkov

Okamoto

et al. 2008

Journal of Medical Microbiology

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Human granulocytic anaplasmosis (HGA) and Lyme borreliosis (LB) are tick-borne infectious diseases caused by Anaplasma phagocytophilum and Borrelia burgdorferi sensu lato species, respectively. In this study, p44/msp2 paralogues specific to A. phagocytophilum and 5S-23S rRNA gene-intergenic spacers specific to B. burgdorferi sensu lato species were detected by PCR in ticks collected in two regions, Tver (Kalinin) and Konakovo, of the Tver (Kalinin) Province located 150 km north-west of Moscow. The PCR amplicons obtained were further characterized by sequencing and RFLP analysis. In the total of 199 ticks collected, 8.8 % (7/80) and 33.8 % (27/80) of Ixodes ricinus, and 2.5 % (3/119) and 45.4 % (54/119) of Ixodes persulcatus, were found to be infected with A. phagocytophilum and B. burgdorferi sensu lato spp., respectively. Of those 199 ticks, 5 (2.5 %) were coinfected with A. phagocytophilum and Borrelia afzelii. Phylogenetic analysis revealed unique p44/msp2 paralogous genes in A. phagocytophiluminfected Russian ticks. The sequence similarities with those of A. phagocytophilum in the United States, UK and Japan ranged from 42 % to 80.4 %, and there were no sequences showing more than 90 % similarity with those sequences from the other countries. The results showed that the p44/msp2 sequence similarity groups may provide an index of adaptation of A. phagocytophilum strains to specific vector ticks or reservoir hosts in different countries and areas. These findings suggest that there is a public health threat from HGA and LB in Tver Province surrounding Moscow. INTRODUCTIONHuman granulocytic anaplasmosis (HGA) and Lyme borreliosis (LB) are tick-borne and emerging infectious diseases caused by Anaplasma phagocytophilum (formerly Ehrlichia phagocytophila, revised by Dumler et al., 2001) and Borrelia burgdorferi sensu lato species. HGA is a febrile systemic illness and the severity of this disease ranges from asymptomatic seroconversion to death. The first case of human infection by A. phagocytophilum was found in the United States in 1994 (Chen et al., 1994). Since then, the number of patients has increased in the United States (Dumler et al., 2005). In Europe, the first human cases of this disease were described in 1997 (Petrovec et al., 1997), and serological and PCR analyses suggest that A. phagocytophilum is distributed throughout Europe and in some parts of the Middle East and Asia (Blanco & Oteo, 2002;Cao et al., 2000; Heo et al., 2002;Keysary et al., 1999). LB is the most common tick-borne infectious disease in the Northern Hemisphere (Masuzawa, 2004;Steere, 2001 METHODSSurvey area and tick sampling. During the summer of 2002, unfed adult ticks (I. persulcatus and I. ricinus) were collected from vegetation by a dragging method using 1 m 2 flannel flags, in the Tver (Kalinin) and Konakovo regions of the Tver Province, which are located 110-150 km north-west from Moscow. Vegetation in the survey area consists of Russian plain and forest (aspen, firs and birches) with bushes. The areas are mostly forest with l...

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“…The percentage of mice found seropositive by IFA for anti-HGE antibodies has been reported to be in the range of 2 to 53% (6,13,16,17,21,23). Dissimilarity in the prevalence of infection with the HGE agent among I. scapularis nymphal and adult stages provides evidence for the role of other mammals in the transmission of this agent to ticks (12). The prevalence of infection with the HGE agent in Peromyscus and the role of these mice as reservoirs may vary geographically (16).…”

Section: Human Granulocytic Ehrlichiosis (Hge) Is a Recently Describementioning

confidence: 99%

Isolation of the Etiologic Agent of Human Granulocytic Ehrlichiosis from the White-Footed Mouse ( Peromyscus leucopus )

et al. 2001

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We examined white-footed mice (Peromyscus leucopus) from Minnesota for infection with the etiologic agent of human granulocytic ehrlichiosis (HGE). From April to September 1997, we collected P. leucopus from Washington County, Minnesota, an area enzootic for HGE. Blood was cultivated in HL60 cells for isolation of the HGE agent. Of 59 mice examined, only a single mouse was culture positive for the HGE agent. The 16S ribosomal DNA sequence of the isolate was determined to be identical to that of the HGE agent. The isolate was reactive with monoclonal antibodies to the 44-kDa antigen of the HGE agent and was infectious for laboratory mice.Human granulocytic ehrlichiosis (HGE) is a recently described granulocytotropic infection first identified in the upper midwestern United States in 1994 (3). HGE is an acute febrile disease that may present as fever, myalgia, arthralgia, headache, and rigors (1, 4). Infection with the etiologic agent of HGE usually responds rapidly to treatment with tetracyclines. However, despite effective therapy, severe cases and some fatalities have occurred (9).Sequences of 16S ribosomal DNA (rDNA) from the HGE agent are nearly identical to those of the granulocytotropic agents Ehrlichia equi and E. phagocytophila (7), which are responsible for zoonotic infections in horses and ruminants, respectively. Serological cross-reactivity between antibodies to the HGE agent and the antigens of E. phagocytophila and E. equi has been demonstrated (8). Infection of horses with the HGE agent follows a clinical course indistinguishable from that of equine granulocytic ehrlichiosis, and horses infected with the agent of HGE are protected against subsequent challenge with E. equi (5).A family of 42-to 49-kDa surface proteins, designated P44, are capable of eliciting immunologic responses in patients with HGE (2,11,19). Genes encoding P44 proteins are members of the granulocytic ehrlichia-MSP-2 multigene family (15) and are present in multiple copies dispersed throughout the genome (24). The expression of P44 homologs has been postulated to be regulated at the level of transcription to maintain antigenic variability (24). P44 sequences from several isolates have been published (10,15,24), and these sequences may suggest that antigenic diversity exists among the species causing HGE.Epidemiological, molecular, and transmission studies provide evidence that Ixodes scapularis is the vector of HGE in the central and eastern United States (14, 18, 22; K. D. Reed, P. D. Mitchell, D. H. Persing, C. P. Kolbert, and V. Cameron, Letter, JAMA 273:23, 1995). Although the natural history of granulocytic ehrlichiosis is not clear, the white-footed mouse, Peromyscus leucopus, has been implicated as a reservoir of the HGE agent. It has been shown that white-footed mice collected from the wild are capable of transmitting ehrlichial organisms to laboratory-reared ticks (22). Serologic and molecular evidence of infection with the E. phagocytophila genomic group has been demonstrated for P. leucopus collected from regions endem...

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Disparity in the Natural Cycles of Borrelia burgdorferi and the Agent of Human Granulocytic Ehrlichiosis

Cited by 45 publications

References 22 publications

Coinfection withBorrelia burgdorferiand the Agent of Human Granulocytic Ehrlichiosis Alters Murine Immune Responses, Pathogen Burden, and Severity of Lyme Arthritis

Coinfection withBorrelia burgdorferiand the Agent of Human Granulocytic Ehrlichiosis Alters Murine Immune Responses, Pathogen Burden, and Severity of Lyme Arthritis

Prevalence of Anaplasma phagocytophilum and its coinfection with Borrelia afzelii in Ixodes ricinus and Ixodes persulcatus ticks inhabiting Tver Province (Russia) – a sympatric region for both tick species

Isolation of the Etiologic Agent of Human Granulocytic Ehrlichiosis from the White-Footed Mouse ( Peromyscus leucopus )

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